Scientists have identified a novel mechanism by which a type of low-carb, low-calorie diet — called a “ketogenic diet” — could delay the effects of aging: the compound β-hydroxybutyrate (βOHB), a “ketone body” that is generated during a prolonged low-calorie or ketogenic diet.

Scientists at the Gladstone Institutes have identified a novel mechanism by which a type of low-carb, low-calorie diet — called a “ketogenic diet” — could delay the effects of aging: the compound β-hydroxybutyrate (βOHB), a “ketone body” that is generated during a prolonged low-calorie or ketogenic diet.

Blocking oxidative stress

While ketone bodies such as βOHB can be toxic when present at very high concentrations in people with diseases such as Type I diabetes, researchers in the laboratory of Gladstone Senior Investigator Eric Verdin, MD found that at lower concentrations, βOHB actually helps protect cells from “oxidative stress” — which occurs as certain molecules build to toxic levels in the body and contributes to the aging process.

This fundamental discovery reveals how such a diet could slow the aging process and may one day allow scientists to better treat or prevent age-related diseases, including heart disease, Alzheimer’s disease, and many forms of cancer.

“Over the years, studies have found that restricting calories slows aging and increases longevity — however the mechanism of this effect has remained elusive,” Dr. Verdin said. He directs the Center for HIV & Aging at Gladstone and is also a professor at the University of California, San Francisco, with which Gladstone is affiliated. “Here, we find that βOHB — the body’s major source of energy during exercise or fasting — blocks a class of enzymes that would otherwise promote oxidative stress, thus protecting cells from aging,” he said.

Oxidative stress occurs as cells use oxygen to produce energy, but this activity also releases other potentially toxic molecules, known as free radicals. As cells age, they become less effective in clearing these free radicals — leading to cell damage, oxidative stress, and the effects of aging.

Slowing the detrimental effects of aging

However, Dr. Verdin and his team found that βOHB might actually help delay this process. In a series of laboratory experiments — first in human cells in a dish and then in tissues taken from mice — the team monitored the biochemical changes that occur when βOHB is administered during a chronic calorie-restricted diet. The researchers found that calorie restriction spurs βOHB production, which blocked the activity of a class of enzymes called histone deacetylases, or HDACs.

Normally HDACs keep a pair of genes, called Foxo3a and Mt2, switched off. But increased levels of βOHB block the HDACs from doing so, which by default activates the two genes. Once activated, these genes kick-start a process that helps cells resist oxidative stress. This discovery not only identifies a novel signaling role for βOHB, but it could also represent a way to slow the detrimental effects of aging in all cells of the body.

“This breakthrough also greatly advances our understanding of the underlying mechanism behind HDACs, which had already been known to be involved in aging and neurological disease,” said Gladstone Investigator Katerina Akassoglou, PhD, an expert in neurological diseases and one of the paper’s co-authors. “The findings could be relevant for a wide range of neurological conditions, such as Alzheimer’s, Parkinson’s, autism and traumatic brain injury — diseases that afflict millions and for which there are few treatment options.”

“Identifying βOHB as a link between caloric restriction and protection from oxidative stress opens up a variety of new avenues to researchers for combating disease,” said Tadahiro Shimazu, a Gladstone postdoctoral fellow and the paper’s lead author. “In the future, we will continue to explore the role of βOHB — especially how it affects the body’s other organs, such as the heart or brain — to confirm whether the compound’s protective effects can be applied throughout the body.”

As the aging population continues to grow, age-related illnesses have become increasingly common. Already in the United States, nearly one in six people are over the age of 65. Heart disease continues to be the nation’s number one killer, with cancer and Alzheimer’s close behind.

Next up...clueless nitwit authors of books claiming "eat all you want: live forever".

SNX weighs in now:

Study seems to support that a ketone body, brought on in conjunction with hypocaloric diets, seems to prevent cell aging.

This does not automatically mean that binge keto eating will still help protect you from aging (certainly doesn't help fat diabetics). That's extrapolation, and it's dangerous. But good for marketing diet books on Amazon.

What is their access to modern medical care like? What do they die from the most? I'm curious.

There are no more true Inuits living their traditional lifestyles any more. All of the villages are modernized now (they hunt using snow mobiles provided by the government, endless supplies shipped into the villages monthly, government built houses etc). If you are 1/16th Native Alaskan, you get free healthcare for life.

They are honestly leaching off of society now, even though they have 10x the opportunities that a normal white citizen would be fortunate enough to encounter. Hardly any of them work legitimate jobs, they all have substance abuse issues, and they keep getting free government checks every month to keep fueling their existence.

No you were serious, now you see it backfires and you trying to weasel yourself out of it you focking cumstain.

it's not like you understand any of this anyways

Quote

Concentrations of acetylcoenzyme A and nicotinamide adenine dinucleotide (NAD+) affect histone acetylation and thereby couple cellular metabolic status and transcriptional regulation. We report that the ketone body D-β-hydroxybutyrate (βOHB) is an endogenous and specific inhibitor of class I histone deacetylases (HDACs). Administration of exogenous βOHB, or fasting or calorie restriction, two conditions associated with increased βOHB abundance, all increased global histone acetylation in mouse tissues. Inhibition of HDAC by βOHB was correlated with global changes in transcription, including the genes encoding oxidative stress resistance factors FOXO3A and MT2. Treatment of cells with βOHB increased histone acetylation at the Foxo3a and Mt2 promoters, and both genes were activated by selective depletion of HDAC1 and HDAC2. Consistent with increased FOXO3A and MT2 activity, treatment of mice with βOHB confered significant protection against oxidative stress.

basically what I'm saying is without any empirical studies it's not going to mean dick in the real world.